AD, one of the most intensively studied forms of neurodegeneration, is
associated with the intracortical formation of proteinaceous plaques containing
large amounts of amyloid beta-peptide (AβP). Morphological evidence
of apoptosis has been observed in AβP-treated cultured neurons201,202 as well
as the cortices of transgenic mice engineered to overexpress AβP.203 More
recently, overexpression of the familial AD gene Presenilin 2 (PS2) has been
reported to increase apoptosis of neuronally differentiated PC12 cells after
NGF withdrawal, exposure to glutamate or treatment with AβP.204-206
Mounting evidence suggests that excessive apoptosis plays a role in